DMA damage checkpoints have evolved to ensure genomic stability, and proteins involved in these signaling pathways are important for tumor suppression. Checkpoint Kinase 1 (Chk1) is an effector kinase involved in phosphorylating and activating substrates involved in cell cycle arrest and DNA repair. Knockout studies in mice have shown that Chk1 is an essential gene as chkl -/- null ES cells display a large number of chromosomal breaks and undergo apoptosis after few cell divisions. Recently Chk1 has been shown to be highly phosphorylated during mitosis, leading us to inquire as to whether Chk1 is involved in mitotic progression. Our preliminary data suggests that Chk1 plays a role in mitosis. Chk1 deficient cells have what appears to be premature mitotic exit. More importantly Cdc25A, an important regulator of mitosis, appears to undergo Chk1-dependent stabilization during mitosis. These results suggest that mitotic, but not interphase, Chk1 promotes stabilization of Cdc25A rather than the normal degradation mediated by Chk1 phosphorylation of Cdc25A during interphase. Further investigation into this pathway can help to elucidate mitotic Chk1 function and help us gain insight into Cdc25A regulation and its role in tumorigenesis.